Gastric acid secretion and lesion formation in rats under water-immersion stress

Hayase, Motohiro; Takeuchi, Koji

doi:10.1007/bf01300703

Cited by 71 publications

(33 citation statements)

References 12 publications

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“…Acid hypersecretion has been noted by some investigators to be associated with lesion formation in water-immersion stressed rats (7,14). However, others have reported either no effects or even suppression of acid secretion (8). In our experiments with pylorus-ligated rats, gastric acid hyper secretion was not found to be a physiological response to restraint and water-immersion stress, indicating that gastric acid secretion was not involved in the pathogenetic mecha nisms of the stress-induced surface epithelial cell damage.…”

Section: Discussionmentioning

confidence: 98%

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Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

et al. 1987

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Abstract-The time-course of gastric mucosal surface epithelial cell damage and macroscopically visible lesions in response to restraint and water-immersion stress (22°C) in rats was examined, and the effects on it of 16,16-dimethyl prostaglandin E 2 (dmPGE2) were compared with those of papaverine, timoprazole and atropine.The stress produced surface epithelial cell damage prior to visible lesion, the former increasing in severity with time and reaching a plateau 60 min later, by which time exfoliation of surface epithelial cells was observable along the mucosal folds. In contrast, macroscopically visible lesions appeared 2 hr after stress, and severity continued to increase with time. Pretreatment injections (s.c.) of dmPGE2 (3, 30 icg/kg), papaverine (100 mg/kg) and atropine (1 mg/kg) protected the surface cells against stress (1 hr)-induced damage, and inhibited visible lesion formation after 4 hr stress. Timoprazole (30 mg/kg, s.c.) did not protect the surface cells, but did markedly inhibit visible lesion formation. dmPGE2, papaverine and atropine, but not timoprazole, inhibited stress-induced increases in gastric contractions. dmPGE2, timoprazole and atropine, but not papaverine, inhibited acid secretion in stress-conditions. These results indicated that stress induced damage to the gastric mucosa within 1 hr due to increased gastric contractions, and the surface epithelial cell damage developed into macroscopically visible lesions in the presence of acid, and that dmPGE2 protected the surface epithelium against stress-induced damage probably by inhibiting gastric contractions.

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Section: Discussionmentioning

confidence: 98%

“…Changes in gastric secretion (7,8), abnormal gastric motility (9,10), and disturbance of gastric mucosal microcircu lation (11,12) have been implicated as underlying pathogenetic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

et al. 1987

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“…Stress itself inhibits gastric acid secretion through a central nervous reflex mechanism (12). Restraint cold stress or restraint water immersion stress induces gastric lesions, which are associated with a decreased or normal level of acid secretion (13,14). Because restraint or water immersion stress significantly decreases acid secretion induced by pylorus ligation (14), acid plays a minor role in stress ulcer.…”

mentioning

confidence: 99%

A Novel Antioxidant and Antiapoptotic Role of Omeprazole to Block Gastric Ulcer through Scavenging of Hydroxyl Radical

Biswas¹,

Bandyopadhyay²,

Chattopadhyay³

et al. 2003

Journal of Biological Chemistry

257

199

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The mechanism of the antiulcer effect of omeprazole was studied placing emphasis on its role to block oxidative damage and apoptosis during ulceration. Dose-response studies on gastroprotection in stress and indomethacin-induced ulcer and inhibition of pylorus ligation-induced acid secretion indicate that omeprazole significantly blocks gastric lesions at lower dose (2.5 mg/kg) without inhibiting acid secretion, suggesting an independent mechanism for its antiulcer effect. Time course studies on gastroprotection and acid reduction also indicate that omeprazole almost completely blocks lesions at 1 h when acid inhibition is partial. The severity of lesions correlates well with the increased level of endogenous hydroxyl radical ( ⅐ OH), which when scavenged by dimethyl sulfoxide causes around 90% reduction of the lesions, indicating that ⅐ OH plays a major role in gastric damage. Omeprazole blocks stress-induced increased generation of ⅐ OH and associated lipid peroxidation and protein oxidation, indicating that its antioxidant role plays a major part in preventing oxidative damage. Omeprazole also prevents stress-induced DNA fragmentation, suggesting its antiapoptotic role to block cell death during ulceration. The oxidative damage of DNA by ⅐ OH generated in vitro is also protected by omeprazole or its analogue, lansoprazole. Lansoprazole when incubated in a ⅐ OH-generating system scavenges ⅐ OH to produce four oxidation products of which the major one in mass spectroscopy shows a molecular ion peak at m/z 385, which is 16 mass units higher than that of lansoprazole (m/z 369). The product shows no additional aromatic proton signal for aromatic hydroxylation in 1 H NMR. The product absorbing at 278 nm shows no alkaline shift for phenols, thereby excluding the formation of hydroxylansoprazole. The product is assigned to lansoprazole sulfone formed by the addition of one oxygen atom at the sulfur center following attack by the ⅐ OH. Thus, omeprazole plays a significant role in gastroprotection by acting as a potent antioxidant and antiapoptotic molecule.

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“…A vast amount of data has shown that gastric acidity is a key contributor to stress-induced gastric mucosal damage induced by RWI [35] . In a previous study [36] , an altered ability of the hypothalamus was suggested to modulate gastric function, including the secretory and motor responses to stress.…”

Section: Discussionmentioning

confidence: 99%

Muscimol microinjection into cerebellar fastigial nucleus exacerbates stress-induced gastric mucosal damage in rats

et al. 2012

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Aim: To investigate the effects of microinjection of the GABA A receptor agonist muscimol into cerebellar fastigial nucleus (FN) on stressinduced gastric mucosal damage and the underlying mechanism in rats. Methods: Stress-induced gastric mucosal damage was induced in adult male SD rats by restraining and immersing them in cold water for 3 h. GABA A receptor agonist or antagonist was microinjected into the lateral FN. The decussation of superior cerebellar peduncle (DSCP) was electrically destroyed and the lateral hypothalamic area (LHA) was chemically ablated by microinjection of kainic acid. The pathological changes in the gastric mucosa were evaluated using TUNEL staining, immunohistochemistry staining and Western blotting. Results: Microinjection of muscimol (1.25, 2.5, and 5.0 µg) into FN significantly exacerbated the stress-induced gastric mucosal damage in a dose-dependent manner, whereas microinjection of GABA A receptor antagonist bicuculline attenuated the damage. The intensifying effect of muscimol on gastric mucosal damage was abolished by electrical lesion of DSCP or chemical ablation of LHA performed 3 d before microinjection of muscimol. Microinjection of muscimol markedly increased the discharge frequency of the greater splanchnic nerve, significantly increased the gastric acid volume and acidity, and further reduced the gastric mucosal blood flow. In the gastric mucosa, further reduced proliferation cells, enhanced apoptosis, and decreased anti-oxidant levels were observed following microinjection of muscimol. Conclusion: Cerebellar FN participates in the regulation of stress-induced gastric mucosal damage, and cerebello-hypothalamic circuits contribute to the process.

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Gastric acid secretion and lesion formation in rats under water-immersion stress

Cited by 71 publications

References 12 publications

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

A Novel Antioxidant and Antiapoptotic Role of Omeprazole to Block Gastric Ulcer through Scavenging of Hydroxyl Radical

Muscimol microinjection into cerebellar fastigial nucleus exacerbates stress-induced gastric mucosal damage in rats

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